Effect of indomethacin on renal function in anaesthetized dogs

Bartha, J

doi:10.1007/bf02082669

Cited by 5 publications

(2 citation statements)

References 19 publications

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“…Inhibition of PG synthesis by IM is fol lowed by a decrease in total RBF, with shifting toward the outer cortical layers both in the isolated canine kidney and in the anaesthetized-laparotomized dog [1,4,5,13,14,25]. In accordance with these findings • Outer and inner cortical blood flow per 100 g kidney.…”

Section: Discussionsupporting

confidence: 76%

Effect of Indomethacin on Renal Function Before and After Release of 24 Hours Unilateral Ureteral Ligation

László¹,

Juszkó²,

Bálint³

1979

Kidney Blood Press Res

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In the anaesthetized dog during and 1 h after release of 24 h unilateral ureteral ligation (UUL) renal blood flow (RBF) decreased to 48 and 43%, respectively, as compared with normal controls. Radioactive microspheres revealed an inward distribution of RBF inasmuch as the ratio outer/inner cortical perfusion (OC/IC) dropped from a control value of 79/21 to 57/43 and 50/50 before and after release, respectively. In normal dogs inhibition of prostaglandin production by indomethacin caused a decrease of RBF with outward distribution, OC/IC amounting to 85/15. Indomethacin treatment in dogs with 24 h UUL led to a further 50% decrease in RBF with a nearly proportional reduction in outer and inner cortical perfusion, with OC/IC ratios amounting to 79/21 before and 74/26 after release. It is assumed that in the ligated kidney prostaglandins produced in the medulla are not transported by the tubular fluid to the outer cortical zones and only exert their dilating effect on the inner cortical, i.e., juxtamedullary, vessels.

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Section: Discussionsupporting

confidence: 76%

Effect of Indomethacin on Renal Function Before and After Release of 24 Hours Unilateral Ureteral Ligation

László¹,

Juszkó²,

Bálint³

1979

Kidney Blood Press Res

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“…Natriuresis has been demonstrated following renal arterial infusion of PGA and PGE [1][2][3][4][5], and this effect can be abolished by PG synthesis inhibitors [6][7][8]. In contrast, other authors observed an increased sodium excretion when PG synthesis inhibitors were administered either to conscious dogs [9], to hypophysectomized dogs [10] or to blood-perfused dog kidneys [II], These discrepan cies may be related to variations in the experimental conditions [12].…”

mentioning

confidence: 97%

Role of Prostaglandins in the Production of Natriuretic Factor by the Isolated Rat Kidney

Cambier¹,

Godon²

1984

Kidney Blood Press Res

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The renal origin of natriuretic factor (NF) of high molecular weight (MW 45,000) has been previously demonstrated. Its role in the control of sodium excretion by the kidney has been strongly suggested. The aim of the present work was to study the relationship between NF and prostaglandins, which are known to modify the renal regulation of sodium. (1) The activity of NF, obtained by ultrafiltration and gel filtration from pooled plasma of salt-loaded rats, was tested on an isolated rat kidney perfused by a cell-free medium. A significant natriuresis was observed in the kidneys isolated either from normal rats or from indomethacin-pretreated rats after injection of NF. Moreover, a dose-response curve was obtained with increasing amounts of NF. (2) The ability of isolated rat kidney to produce NF was studied in two series of salt-deprived rats, the second series being pretreated with indomethacin. The production of NF by isolated kidneys was induced by addition of saline to the fluid perfusing kidneys isolated from normal or indomethacin-pretreated rats fed a salt-depleted diet. Before addition of saline, no natriuretic activity was detectable. After the addition of 0.9% NaCl, NF was only found in the perfusate from kidneys isolated from normal rats. Perfusate extracts from indomethacin-pretreated kidneys did not induce any significant rise in natriuresis. (3) Kidneys isolated from rats previously fed a free fatty acid-deficient diet and thus prostaglandin-depleted were unable to produce NF even if they were salt-loaded. Intraarterial perfusion of prostaglandin E₂ restored their ability to release or secrete NF. It is concluded that the release or the synthesis of NF is only possible in the presence of prostaglandins. Its action is not influenced by prostaglandin inhibition or deficiency.

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The effect of indomethacin on kidney function: Indomethacin and furosemide antagonism

Kövér

Tost

1977

Pflugers Arch.

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The effect of furosemide and indomethacin on renal function was investigated in anesthetized dogs. 1. On infusing 0.05 mg/kg/min furosemide directly into the left renal artery, about 18% of the filtered water and 19% of the filtered sodium was excreted in both non-hydrated and hydrated dogs. 2. Under the effect of 0.1 mg/kg/min indomethacin administered intravenously renal blood flow decreased markedly, glomerular filtration rate remained unchanged, the filtration fraction increased. 3. Indomethacin induced a decrease in water and sodium rejection and water and sodium excretion in both the hydrated and non-hydrated animals. 4. Indomethacin inhibited the diuretic effect of furosemide in the non-hydrated animals. This effect was much weaker in the hydrated group. These data suggest that in the anesthetized dog, endogenous prostaglandins may serve to maintain renal blood flow but not glomerular filtration rate. It is concluded that the indomethacin-induced inhibition of the furosemide effect is the consequence of hemodynamic changes occurring in the kidney. The data do not support the direct physiological role of prostaglandins in regulating tubular function.

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Effect of indomethacin on renal function in anaesthetized dogs

Cited by 5 publications

References 19 publications

Effect of Indomethacin on Renal Function Before and After Release of 24 Hours Unilateral Ureteral Ligation

Effect of Indomethacin on Renal Function Before and After Release of 24 Hours Unilateral Ureteral Ligation

Role of Prostaglandins in the Production of Natriuretic Factor by the Isolated Rat Kidney

The effect of indomethacin on kidney function: Indomethacin and furosemide antagonism

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